Atrial tachyarrhythmias (AT) affect many people and the quality of their lives. For instance, atrial fibrillation (AF) affects an estimated 2.3 million people in the United States. AF is a condition in which control of heart rhythm is taken away from the normal sinus node pacemaker by rapid activity (400-600 pulses per minute in humans versus about 60 beats/minute at rest or 180-200 beats/minute at peak exercise) in different areas within the upper chambers (atria) of the heart. This results in rapid and irregular atrial activity and, instead of contracting, the atria quiver. It is the most common chronic cardiac rhythm disturbance in humans and represents a major clinical problem with serious morbidity and mortality. AF requires a trigger and an atrial substrate to perpetuate AF. Eliminating the trigger or altering the substrate may reduce the incidence of AF. A substrate that perpetuates AF may involve the wavelength (conduction velocity, CV; and effective refractory period, ERP). Altering either CV or ERP may change the substrate necessary to maintain AF. Moreover, short atrial ERPs contribute to the substrate for multiple reentrant wavelets that sustain AF.
Pharmacological and device therapies have not been satisfactory to treat AF, as they have varying degrees of efficacy as well as side effects and complications. Cardiac arrhythmias have been treated traditionally with antiarrhythmic drugs that control the rhythm by altering cardiac electrical properties. However, the available drugs are not specific for atrial electrical activity and can have profound effects on ventricular electrophysiology. For example, K channel blocking drugs that are used to treat AF can mimic potentially lethal congenital disorders of the cardiac repolarization (Such as “torsade-de-pointes”). Moreover, it has become apparent over the last 20 years that the effects of antiarrhythmic drugs on the electrophysiology of the ventricles can themselves paradoxically lead to life-threatening rhythm disorders (proarrhythmia) and increase mortality. Further, drug therapy has only about 60% efficacy. There has been, therefore, a shift towards non-pharmacological therapies for cardiac arrhythmias, including controlled destruction of arrhythmia-generating tissue (“ablation therapy”) and implantable devices that can sense arrhythmias and terminate them with controlled electrical discharges. However, catheter-based therapies have less than ideal efficacy and are often very time consuming due to the need to maintain adequate catheter position and contact for extended times, inconsistency in the extent of ablation with distance from the site of delivery, and multiple ablations are generally required to form the desired physical extent of ablation. In contrast to other cardiac arrhythmias, AF continues to be challenge for both pharmacological and non-pharmacological approaches to treatment.